Background: Drug-induced liver injury is an uncommon, idiosyncratic adverse reaction with heterogeneous clinical presentations, ranging from asymptomatic transaminase elevations to acute liver failure. Sodium-glucose cotransporter 2 inhibitors, widely prescribed for type 2 diabetes due to their glycaemic, cardiovascular, and renal benefits, are generally considered safe to the liver. Nonetheless, rare cases of cholestatic and hepatocellular drug-induced liver injury have been reported, highlighting the need for vigilance and systematic evaluation when liver dysfunction occurs in patients receiving these agents. Case report: We describe a 56-year-old man with type 2 diabetes and chronic schizophrenia who developed cholestatic liver injury 36 days after initiating empagliflozin 10 mg od. The patient presented with jaundice, dark urine, and pale stools, with laboratory findings revealing elevated bilirubin, gamma-glutamyl transferase, and alkaline phosphatase disproportionate to alanine aminotransferase. Comprehensive work-up excluded viral, autoimmune, metabolic, and obstructive causes. Imaging confirmed intrahepatic cholestasis without biliary obstruction. Causality assessment using the Roussel Uclaf Causality Assessment Method, Maria and Victorino and Naranjo scores indicated probable adverse drug reaction. Liver biopsy demonstrated acute cholestatic injury with portal inflammatory infiltrates and ductular reaction, consistent with drug-related pathology. Empagliflozin withdrawal led to gradual clinical and biochemical recovery. Conclusion: Empagliflozin can, in rare cases, trigger idiosyncratic cholestatic drug-induced liver injury, even in patients with cirrhosis. Early recognition, prompt drug withdrawal, and systematic evaluation are essential. This case adds to the limited literature on sodium-glucose cotransporter 2 inhibitor-associated hepatotoxicity.

Background: Spontaneous intracranial hypotension (SIH) is a rare, underdiagnosed cause of secondary headache due to cerebrospinal fluid (CSF) leakage. While typically presenting with orthostatic headache, atypical manifestations may mimic infectious or inflammatory diseases. Case description: A 45-year-old man presented with acute alteration of consciousness, expressive aphasia, and nuchal rigidity after 1 month of orthostatic occipital headache. Brain magnetic resonance imaging (MRI) showed diffuse pachy- and leptomeningeal enhancement initially interpreted as infectious meningoencephalitis. Lumbar puncture revealed turbid, blood-stained CSF with elevated protein and neutrophilic pleocytosis, but microbiological and autoimmune studies were negative. Neurological symptoms improved with conservative management (bed rest, hydration, analgesia), and follow-up imaging confirmed full resolution. Retrospective neuroradiological review reclassified findings as SIH. Conclusion: SIH can mimic infectious meningoencephalitis both clinically and in CSF appearance. Recognition of preceding orthostatic headache and characteristic MRI features is essential to avoid unnecessary antimicrobial therapy and invasive diagnostic procedures.

Background: Streptococcus pneumoniae is a leading cause of community-acquired pneumonia and meningitis, but intra-abdominal manifestations are rare, particularly in adults without underlying peritoneal disease. Primary pneumococcal peritonitis is classically associated with cirrhosis, nephrotic syndrome, or peritoneal dialysis, and has seldom been reported in patients with haematological malignancies. Multiple myeloma significantly increases the risk of invasive pneumococcal disease due to impaired humoral immunity and hypogammaglobulinemia. Case report: We report a 40-year-old woman with smouldering IgG lambda multiple myeloma presenting with abdominal pain, diarrhoea, vomiting, and hypotension. Laboratory tests revealed macrocytic anaemia, leukopenia with absolute neutropenia, acute kidney injury, elevated inflammatory markers, and compensated metabolic acidosis. A computed tomography (CT) scan of the abdomen and pelvis showed partially loculated ascites, peritoneal fat stranding, and thickening of duodenum, descending, and sigmoid colon walls. Blood cultures were positive for Streptococcus pneumoniae, confirming atypical invasive pneumococcal disease manifesting as spontaneous primary peritonitis with secondary enterocolitis. Despite broad-spectrum antibiotics, the patient developed persistent sepsis complicated by multiple intra-abdominal abscesses. Echocardiography and a spine CT scan excluded endocarditis or vertebral involvement. Source control was achieved through three ultrasound-guided percutaneous drainage procedures, resulting in gradual clinical and radiological resolution. She was discharged on day 42 with complete recovery and scheduled pneumococcal vaccination. Conclusion: This case highlights a rare and severe gastrointestinal manifestation of invasive pneumococcal disease in a high-risk host. Spontaneous pneumococcal peritonitis complicated by multiple intra-abdominal abscesses is exceptionally uncommon in multiple myeloma. Early recognition, multidisciplinary management, and minimally invasive source control were crucial to a favourable outcome. Preventive strategies, particularly pneumococcal vaccination, remain essential to reduce morbidity in immunocompromised patients.

Background: Systemic mastocytosis is a rare clonal disorder characterised by the proliferation and accumulation of mast cells in one or more extracutaneous organs. Its clinical presentation is highly heterogeneous and aggressive variants may mimic metastatic malignancy, leading to significant diagnostic delay. Case description: We report the case of an 83-year-old woman presenting with fatigue, weight loss, low-grade evening fever and night sweats over two months. Laboratory evaluation showed pancytopenia, mild inflammatory response, and normal hepatic and renal function. Imaging studies revealed diffuse osteoblastic lesions throughout the axial skeleton, initially interpreted as bone metastases from an unknown primary tumour. Further imaging demonstrated hepatosplenomegaly and prominent periportal lymph nodes. Bone biopsy of an iliac lesion revealed replacement of marrow by sheets of epithelioid mast cells (CD117+, tryptase, CD68+). Serum tryptase was elevated (56.3 ng/ml), fulfilling World Health Organization (WHO) diagnostic criteria for systemic mastocytosis. The patient was diagnosed with aggressive systemic mastocytosis and started cladribine therapy with antimicrobial prophylaxis, with progressive improvement of constitutional symptoms and she remains under follow-up in the haematology department. Discussion: Aggressive systemic mastocytosis presenting with diffuse osteoblastic bone lesions is extremely uncommon and may closely mimic metastatic carcinoma, particularly of breast or prostate origin. Diagnosis requires a high index of suspicion and confirmation through histopathology, immunophenotyping and serum tryptase measurement. KIT mutations, especially D816V, are frequent but were absent in this case. Conclusion: This case highlights the importance of considering systemic mastocytosis in the differential diagnosis of osteoblastic bone disease, particularly in elderly patients with constitutional symptoms and unexplained cytopenias. Early recognition allows timely initiation of appropriate therapy and avoids unnecessary oncology investigations.